The first, most obvious sign of CWD is the progressive loss of weight and body condition over time, despite continued feeding activity. In the latter stages, infected animals may drink and urinate an unusual amount. Behavior is altered significantly by the disease, and may include sluggishness, decreased activity, blank-expressions, and repetitive movement patterns. In some cases, watering at the mouth and grinding of teeth are observed. The disease incubates up to 16 months in animals before clinical signs may be noticed, then typically sheds starting from 16–36 months . More recent research indicates that transmission is possible through prions shed in feces prior to 16 months . Therefore, it is possible for it to be transferred from apparently healthy individuals. It should be noted, however, that the presence of these symptoms, however, is not a clear diagnosis of the disease.
CWD is most transmitted from animal-to-animal through direct or indirect exposure, although transmission from mothers to offspring at birth may occur . Typically, animals are 3–4 years old before clinical signs appear, but there are cases documented with animals as young as 18 months up to 13 years at first sign of symptoms. It is highly uncommon for yearlings to exhibit any clinical signs. CWD is passed through contact with feces, urine, or saliva. Some speculation exists that males may be exposed to transmission during annual removal of antler velvet by rubbing of this soft tissue on structures in the environment. The shedding of infectious agents into the environment after death from carcasses is likely equally important. Recent research indicates that certain plant structures may efficiently bind and retain infected prions from these transmission routes, thereby preserving them in the environment and acting as reservoirs for the disease.
As previous efforts to eradicate CWD from captive cervid facilities have proved, the infectious agents remain active in the environment for a long time, and are difficult to remove. Thus, indirect transmission may be just as important as direct transmission. Thus, areas of high cervid density, such as holding pens in captive facilities, or supplemental feeding stations, may serve as transmission hot-spots or sources for infection of herds. The movement of animals accomplishes long-distance transmission of the disease. Although some speculate that initial transmission likely occurred from captive cervids contacting wild populations, there is no clear evidence to support this assertion. Furthermore, it is likely that transmission has now occurred both from and to wild populations. Transmission from cervids to domestic livestock, however, is unlikely to develop.